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HU, Y.

Publications and source records attributed to HU, Y..

4 recordsLinked to original sources

Overcoming Topology Bias and Cold-Start Limita-tions in Drug Repurposing: A Clinical-Outcome-Aligned LLM Framework

Graph Neural Networks (GNNs) in drug repurposing suffer from two limitations: transductive failure in zero-shot (cold-start) scenarios and popularity bias that misidentifies high-degree nodes as effective drugs. We propose a framework that shifts the optimization objective from graph topology to clinical utility, integrating Knowledge Graph RAG (KG-RAG), Supervised Fine-Tuning (SFT), and Kahneman-Tversky Optimization (KTO) using Phase III clinical trial outcomes as rewards. We evaluated our approach on a rigorous 1:10 negative sampling benchmark derived from MiRAGE, covering Standard, Cold-Start, and Degree-Matched settings. In Cold-Start scenarios where topological signals are absent, traditional GNNs (including TxGNN) collapse (Top-10 Precision < 0.30), whereas DR-SFT model achieves 0.80, demonstrating robust semantic generalization for novel compounds. Crucially, in Degree-Matched tests dominated by "popular but ineffective" decoys, the DR-KTO acts as a clinical gatekeeper, achieving 0.90 Top-10 Precision--significantly outperforming DR-SFT (0.70) and GNNs (0.2-0.4) by effectively penalizing hard negatives. Beyond repurposing accuracy, the model achieves state-of-the-art performance on BioASQ, and increased ability in Chemprot. Orthogonal validation via DrugReAlign confirms physical plausibility, yielding significantly lower docking binding energies for KTO-recommended candidates. SPR experiments further corroborate these findings. By aligning LLM reasoning with clinical evidence, our framework successfully bridges the gap between semantic inference, topological structure, and clinical reality.

pharmacology and toxicology↗

FSCN1-Mediated Hepatic Gluconeogenesis Is Indispensable for Neonatal Mice Survival

Actin-Bundling Protein Fascin1 (FSCN1) is encoded by the Fscn1 gene, and crucial for cytoskeletal remodeling and cellular migration. While previous study linked Fscn1 deficiency to neonatal lethality in mice, the underlying metabolic mechanism remains unexplored. Here, in this study, we report that systemic knockout (KO) of Fscn1 leads to 52.2% mortality within 24 hours post-birth, accompanied by severe hypoglycemia in KO pups compared to other littermates. Remarkably, this lethality was fully rescued by oral glucose administration, indicating a glucose supply-dependent survival mechanism. Surviving Fscn1 KO neonates displayed persistent developmental deficits, including growth retardation and depleted lipid stores, despite intact canonical insulin-regulated hepatic gluconeogenic pathways. Transcriptomic profiling of P0 livers revealed that Fscn1 loss predominantly disrupts metabolic pathway, within the glycerol phosphate shuttle being the most significantly downregulated module. Mechanistically, Fscn1 KO livers exhibited markedly reduced protein levels of glycerol-3-phosphate dehydrogenase isoforms (GPD1/GPD2), key enzymes bridging glycolysis and gluconeogenesis. Consistently, glycerol tolerance tests (GTT) demonstrated impaired glycerol-to-glucose conversion in Fscn1 KO mice, confirming defective glycerol-driven gluconeogenesis. Our findings establish FSCN1 as a novel cytoskeletal-metabolic integrator essential for neonatal survival by sustaining hepatic glucose production from glycerol, thus revealing an unexpected role of actin dynamics in coordinating metabolic adaptation during early postnatal development. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=184 HEIGHT=200 SRC="FIGDIR/small/654691v1_ufig1.gif" ALT="Figure 1"> View larger version (34K): org.highwire.dtl.DTLVardef@b4fb56org.highwire.dtl.DTLVardef@1e0f47forg.highwire.dtl.DTLVardef@1d3cb1eorg.highwire.dtl.DTLVardef@1bc6022_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIFSCN1 deficiency triggers hypoglycemia-driven neonatal mortality by disrupting hepatic glucose production. C_LIO_LIFscn1 loss impairs the gluconeogenesis via suppressing GPD1/GPD2 expression, while sparing insulin-regulated gluconeogenesis. C_LIO_LICytoskeletal dysfunction impairs glycerol-to-glucose conversion, revealing actin-metabolism crosstalk in postnatal adaptation. C_LI

molecular biology↗

CSTA: A Biomarker Regulating Esophageal Stricture Epithelial Barrier, Potential Medication Target

Esophageal strictures resulting from ESD/EMR in the esophagus are distressing, with uncertain causes and treatments due to epithelial barrier dysfunction. We explored cystatin A (CSTA) as a novel biomarker for the esophageal epithelial barrier. CSTA regulates the barrier and is influenced by tacrolimus (FK506). Analyzing biopsy samples by proteomics, we identified CSTA as an esophageal epithelial biomarker. Knocking down CSTA reduced responsiveness to triamcinolone acetonide (TA) and lowered expression of proteins related to cell-cell junctions and barrier function during inflammation. These findings suggest that down-regulate CSTA weakens tight junctions and the esophageal barrier, leading to strictures. Notably, FK506 showed promise in rescuing CSTA-knockdown cells by increasing the expression of proteins related to cell-cell junctions and barrier function. This highlights FK506 as a potential therapy for esophageal strictures in patients with CSTA mutations.

cell biology↗

Endocast and bony labyrinth of a stem gnathostome shed light on the earliest diversification of jawed vertebrates

Our understanding of the earliest evolution of jawed vertebrates depends on a credible phylogenetic assessment of the jawed stem gnathostomes collectively known as placoderms. However, their relationships, and even whether placoderms represent a single radiation or a paraphyletic array, remain contentious. Here we describe the endocranial cavity and inner ear of Brindabellaspis stensioi, commonly recovered as a taxon of uncertain affinity branching near the base of placoderms. While some features of its braincase and endocast resemble those of jawless vertebrates, its inner ear displays a repertoire of crown gnathostome characters. Both parsimony and Bayesian analyses suggest that established hypotheses of placoderm relationships are unstable, with newly-revealed anatomy pointing to a potentially radical revision of early gnathostome evolution. Our results call into question the appropriateness of fusiform placoderms as models of primitive gnathostome anatomy and raise questions of homology relating to key cranial features. One Sentence SummaryThe skull of a 400-million-year old fossil fish suggests that hypotheses of early jawed vertebrate relationships might have to be turned on their head.

paleontology↗